首发精神分裂症患者的血清同型半胱氨酸水平及其与P_(300)的关系

目的研究首发精神分裂症患者血清同型半胱氨酸(Homocysteine,Hcy)与事件相关电位P300和临床症状之间的关系。方法采用丹麦KeyPointV2.12脑电生理仪对42例首发精神分裂症患者及28名正常对照进行P300测查,高效液相色谱法测定血清同型半胱氨酸浓度,阳性和阴性症状量表(PANSS)评定患者的临床症状。结果患者组血清Hcy水平高于正常对照组,差异有统计学意义(P0.01)。与对照组比较,患者组P300波幅在Fz点降低(P0.01)。相关分析显示,患者组血清Hcy水平与Fz点的P300波幅呈负相关(r=-0.37,P0.05),而与Pz点的P300潜伏期呈正相关(r=0.34,P0.05);患者组血清Hcy水平与PANSS阴性症状分呈正相关(r=0.49,P0.01);患者组PANSS阴性症状分与Fz点的P300波幅呈负相关(r=-0.39,P0.05)。结论首发精神分裂症患者血清Hcy水平升高,Hcy代谢失衡与精神分裂症的认知功能损害有关。     

精神分裂症患者事件相关电位研究

目的 :研究以阴性、阳性症状为主的精神分裂症患者的事件相关电位 (ERPs)。　方法 :将 2 2例阴性、 2 7例阳性未服药的精神分裂症患者和 17例正常对照组 ,进行 N1 0 0 、 P2 0 0 、 N2 0 0 、 P30 0 测查。　结果 :阴性组在 Fz,Cz,Pz,T7,T85个点的 P30 0 波幅显著低于和潜伏期明显长于正常对照组 ;阳性组在 Cz,Pz点的 P30 0 波幅低于正常对照组 (P<0 .0 5 )。 P30 0 的波幅与潜伏期在两组患者之间差异有显著性 (P<0 .0 5 ) ;阴性患者 N1 0 0 、N2 0 0 的波幅低于正常对照组 ;相关分析发现 ,阴性分量表分与 Fz的 P30 0波幅显著负相关 (r=— 0 .31,P<0 .0 5 ) ,与 T7、 T8点的潜伏期呈显著正相关 (r=0 .33,r=0 .35 ,P<0 .0 5 )。　结论 :以阳性、阴性症状为主的精神分裂症可能有不同的神经生物学基础。     

精神分裂症首发患者的非匹配负波及P300随访研究

目的了解精神分裂症首发患者非匹配负波（MMN）和P300的特征以及治疗缓解后脑电波的变化。方法应用美国Bravo脑电生理仪,比较58例首发分裂症患者和54名健康人的MMN和P300电位,并用阳性和阴性症状量表（PANSS）评定患者精神症状。患者组于治疗5周和14周时随访MMN和P300。结果①精神分裂症首发患者组的MMN潜伏期[（222.4±33.0）ms]比正常对照组[（200.5±30.1）ms]延迟（t=3.66,P〈0.01）,波幅[（4.6±3.3）μV]比对照组[（7.9±3.9）μV]低（t=4.85,P〈0.01）。患者组P300中靶潜伏期P3同时延迟;②MMN潜伏期延长和波幅低,与PANSS阳性症状和思维障碍分呈负相关（r=-0.381,P〈0.05,r=-0.459,P〈0.01）;患者组经治疗14周后,MMN波幅呈增大改变和潜伏期缩短。结论MMN和P300联合应用可能作为精神分裂症首发患者临床检测指标。     

精神分裂症患者脑源性神经营养因子与事件相关脑电位N400的相关性研究

目的:探讨精神分裂症患者脑源性神经营养因子(BDNF)与事件相关脑电位N400和临床症状之间的关系。方法:对58例精神分裂症患者(患者组)及60名健康对照(正常对照组)进行N400测查,采用酶联夹心免疫吸附法测定血清BDNF水平。使用阳性和阴性症状量表(PANSS)评定患者的临床症状。结果:患者组血清BDNF水平低于正常对照组,差异有统计学意义(P0.05)。在Fz点,患者组N400中异音形似异义的匹配潜伏期延迟(P0.05);N400中异音异形同义的匹配潜伏期和波幅以及非匹配波幅下降(P0.05或P0.01)。BDNF水平变化值与PANSS总分及各因子分变化值无相关性(P均0.05)。患者组血清BDNF水平与Fz点N400波幅与潜伏期呈正相关(P0.05或P0.01)。结论:精神分裂症患者血清BDNF水平降低与其N400变异及认知功能损害有关。     

重复经颅磁刺激对精神分裂症患者事件相关电位的影响

目的:探讨重复经颅磁刺激(rTMS)对精神分裂症患者失匹配负波(MMN)及P300的影响。方法:应用美国脑电生理仪器,对78例精神分裂症患者在rTMS治疗前后进行P300和MMN检测,观察rTMS治疗前后P300和MMN的变化。结果:与正常组比较,精神分裂症组MMN潜伏期延迟,和波幅降低(P0.05或P0.01),P300中的靶波幅P3降低(P0.05)。患者组经过25次rTMS治疗后MMN波幅及P300靶波幅P3明显提高(P0.05或P0.01)。结论:rTMS治疗可以提高精神分裂症患者事件相关电位的MMN及P3波幅。     

重复经颅磁刺激对精神分裂症患者事件相关电位的影响

目的观察重复经颅磁刺激(rTMS)治疗前后精神分裂症患者的失匹负波(MMN)及P300的变化特点。方法对78例精神分裂症患者(精神分裂症组)在rTMS治疗前后进行了P300和MMN检测,观察rTMS治疗前后P300和MMN的变化。另对62名正常对照者(对照组)进行P300和MMN检测,并将两组结果进行比较。结果与对照组相比,精神分裂症组的MMN潜伏期延迟和波幅降低(分别P0.05和P0.01),P300中的靶波幅P3降低(P0.05)。精神分裂症组经过rTMS治疗后,MMN波幅及P300靶波幅P3较治疗前有所恢复(P0.05)。结论联合应用P300和MMN,可作为抗精神病药物合并rTMS治疗精神分裂症的疗效监测指标。     

缺陷型及非缺陷型精神分裂症首次发病未服药患者失匹配负波的对照研究

目的:探讨缺陷型与非缺陷型精神分裂症首次发病未服药患者失匹配负波(MMN)的特征及与临床状态的相关性。方法:根据缺陷型精神分裂症诊断量表评分将100例首发精神分裂症患者分为缺陷型(缺陷组,45例)和非缺陷型(非缺陷组,55例);采用脑诱发电位仪检测MMN,并与50名正常对照者(对照组)比较;分析患者MMN改变与其发病年龄、病程、病情及功能的关系。结果:与对照组比较,缺陷组与非缺陷组MMN潜伏期明显延长(F=21.72,P=0.00),波幅明显降低(F=5.95,P=0.00);缺陷组与非缺陷组间MMN潜伏期及波幅差异无统计学意义(P均>0.05)。患者的MMN潜伏期及波幅与的其发病年龄、病程、阳性和阴性症状量表(PANSS)评分(包括总分、阳性症状分、阴性症状分、一般精神病理分)及大体功能评定量表(GAF)评分无显著相关性(P均>0.05)。结论:缺陷型和非缺陷型首发精神分裂症患者均存在MMN异常;其可能是精神分裂症患者的素质性标记。     

重复经颅磁刺激对精神分裂症患者事件相关电位的影响

目的:探讨重复经颅磁刺激(rTMS)对精神分裂症患者事件相关脑电位(ERPs) N400、P300和失匹配负波(MMN)的影响。方法:给予85例精神分裂症患者(患者组)在原抗精神病药治疗的基础上联合rTMS治疗25次;于rTMS治疗前后进行N400、P300及MMN检测,结果进行自身对照及与76名健康志愿者(正常对照组)比较。结果:与正常对照组比较,患者组额区N400、P300和MMN潜伏期明显延迟、波幅明显降低(P 0.05或P 0.01);治疗后患者额区N400中同音异形异义潜伏期和异音异形异义波幅、额区MMN及P300波幅较治疗前明显提高(P均0.05)。结论:精神分裂症患者ERP指标异常,经rTMS治疗可明显改善N400、P300和MMN。     

精神分裂症患者脑电失匹配负波的对照研究

目的探讨精神分裂症患者失匹配负波(mismatch negativity,MMN)的特点以及治疗后MMN的变化。方法应用美国Bravo脑电生理仪,记录43例精神分裂症患者和36名正常人的MMN,同时记录P300电位比较。患者组于治疗6周和15周时进行MMN随访。结果(1)与正常组比较,精神分裂症组的MMN潜伏期延迟和波幅降低[正常组(198.5±27.4)ms和(7.9±3.6)μV,患者组(224.9±33.8)ms,(4.6±3.3)μV,P均<0.01],患者组P300中靶潜伏期P3同时延迟(P<0.01)。(2)患者组经治疗15周后,MMN波幅呈增大改变和潜伏期缩短(P<0.01),反映患者的认知功能改善。结论MMN技术可反映精神分裂症患者诱发脑电的自动加工过程。MMN可作为精神分裂症患者的临床应用检测指标之一。     

精神分裂症与强迫症错误监控功能改变的比较研究

目的:探讨精神分裂症和强迫症患者错误相关负电位(ERN)变化特征及与临床症状的相关性。方法:对64例精神分裂症和59例强迫症患者及56名健康成人进行ERN检测、阳性与阴性症状量表(PANSS)及耶鲁-布朗强迫量表(Y-BOCS)评估,并对结果进行相关分析比较。结果:精神分裂症组和强迫症组ERN的正确反应率明显低于正常对照组;正确反应和错误反应的反应时明显长于正常对照组(P均0.01)。与正常对照组相比,精神分裂症组ERN波幅降低、潜伏期延长,强迫症组ERN波幅增高(P0.05或P0.01)。ERN潜伏期和波幅变化与精神分裂症阳性症状及PANSS总分(r=0.088,P0.05)、强迫症组ERN波幅与Y-BOCS评分之间不相关(r=0.117,P0.05)。结论:精神分裂症的ERN波幅降低及强迫症的ERN波幅增高可能反映两组患者内在错误监控机制存在缺陷。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -